Akinloye Bankole Oyetunde1 
,
Ayodeji O Olayanju1, 2,
Adeola O Oluboyo1,
Emmanuel A Omon1,
Chisara S Okolo1,
Yashim A Nuhu3,
Ayuba Sunday Buru4
For correspondence:- Akinloye Oyetunde Email: oyetundeab@pg.abuad.edu.ng
Received: 2 June 2025 Accepted: 14 December 2025 Published: 28 December 2025
Citation: Oyetunde AB, Olayanju AO, Oluboyo AO, Omon EA, Okolo CS, Nuhu YA, et al. Assessment of oxidative stress biomarkers in steady and crisis states of sickle cell disease. Trop J Pharm Res 2025; 24(12):1469-1477 doi: https://dx.doi.org/10.4314/tjpr.v24i12.2
© 2025 The authors.
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Purpose: To assess the oxidative stress parameters in steady and crisis state patients with sickle cell disease (Hb SS) in Nigeria, which has the highest prevalence of the monogenetic disorder. Methods: Blood specimens were collected from 100 Hb SS participants (comprising 50 in steady state, 50 in crises with > three transfusions in a year) and 50 Hb AA apparently healthy, non-transfused controls with normal blood values between January 2023 to June 2024. Malondialdehyde (MDA), superoxide dismutase (SOD) Catalase levels in plasma were determined using Enzyme-Linked Immunosorbent Assay (ELISA). Results: Superoxide dismutase (SOD) and catalase were significantly lower (p < 0.05), while malondialdehyde was significantly higher in sickle cell subjects compared to control group (p < 0.05). Catalase levels were reduced in crises and steady state sickle cell disease (SCD) compared to control group. The SOD was significantly higher in female subjects in both steady state and crisis (p < 0.05). There was no significant difference in Catalase (CAT) and Superoxide dismutase (SOD) with respect to gender and age (p > 0.05). Conclusion: There is evidence of an increase in oxidative stress in individuals with SCD. The further reduction in antioxidant capacity during VOC relative to steady state underscores that oxidative damage is significantly aggravated during acute crises. This suggests that excessive generation of reactive oxygen species (ROS) and reduced antioxidant defense mechanisms contribute substantially to the pathophysiology of sickle cell anemia.
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